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Guru Granth Sahib
Composition, Arrangement & Layout
ਜਪੁ | Jup
ਸੋ ਦਰੁ | So Dar
ਸੋਹਿਲਾ | Sohilaa
ਰਾਗੁ ਸਿਰੀਰਾਗੁ | Raag Siree-Raag
Gurbani (14-53)
Ashtpadiyan (53-71)
Gurbani (71-74)
Pahre (74-78)
Chhant (78-81)
Vanjara (81-82)
Vaar Siri Raag (83-91)
Bhagat Bani (91-93)
ਰਾਗੁ ਮਾਝ | Raag Maajh
Gurbani (94-109)
Ashtpadi (109)
Ashtpadiyan (110-129)
Ashtpadi (129-130)
Ashtpadiyan (130-133)
Bara Maha (133-136)
Din Raen (136-137)
Vaar Maajh Ki (137-150)
ਰਾਗੁ ਗਉੜੀ | Raag Gauree
Gurbani (151-185)
Quartets/Couplets (185-220)
Ashtpadiyan (220-234)
Karhalei (234-235)
Ashtpadiyan (235-242)
Chhant (242-249)
Baavan Akhari (250-262)
Sukhmani (262-296)
Thittee (296-300)
Gauree kii Vaar (300-323)
Gurbani (323-330)
Ashtpadiyan (330-340)
Baavan Akhari (340-343)
Thintteen (343-344)
Vaar Kabir (344-345)
Bhagat Bani (345-346)
ਰਾਗੁ ਆਸਾ | Raag Aasaa
Gurbani (347-348)
Chaupaday (348-364)
Panchpadde (364-365)
Kaafee (365-409)
Aasaavaree (409-411)
Ashtpadiyan (411-432)
Patee (432-435)
Chhant (435-462)
Vaar Aasaa (462-475)
Bhagat Bani (475-488)
ਰਾਗੁ ਗੂਜਰੀ | Raag Goojaree
Gurbani (489-503)
Ashtpadiyan (503-508)
Vaar Gujari (508-517)
Vaar Gujari (517-526)
ਰਾਗੁ ਦੇਵਗੰਧਾਰੀ | Raag Dayv-Gandhaaree
Gurbani (527-536)
ਰਾਗੁ ਬਿਹਾਗੜਾ | Raag Bihaagraa
Gurbani (537-556)
Chhant (538-548)
Vaar Bihaagraa (548-556)
ਰਾਗੁ ਵਡਹੰਸ | Raag Wadhans
Gurbani (557-564)
Ashtpadiyan (564-565)
Chhant (565-575)
Ghoriaan (575-578)
Alaahaniiaa (578-582)
Vaar Wadhans (582-594)
ਰਾਗੁ ਸੋਰਠਿ | Raag Sorath
Gurbani (595-634)
Asatpadhiya (634-642)
Vaar Sorath (642-659)
ਰਾਗੁ ਧਨਾਸਰੀ | Raag Dhanasaree
Gurbani (660-685)
Astpadhiya (685-687)
Chhant (687-691)
Bhagat Bani (691-695)
ਰਾਗੁ ਜੈਤਸਰੀ | Raag Jaitsree
Gurbani (696-703)
Chhant (703-705)
Vaar Jaitsaree (705-710)
Bhagat Bani (710)
ਰਾਗੁ ਟੋਡੀ | Raag Todee
ਰਾਗੁ ਬੈਰਾੜੀ | Raag Bairaaree
ਰਾਗੁ ਤਿਲੰਗ | Raag Tilang
Gurbani (721-727)
Bhagat Bani (727)
ਰਾਗੁ ਸੂਹੀ | Raag Suhi
Gurbani (728-750)
Ashtpadiyan (750-761)
Kaafee (761-762)
Suchajee (762)
Gunvantee (763)
Chhant (763-785)
Vaar Soohee (785-792)
Bhagat Bani (792-794)
ਰਾਗੁ ਬਿਲਾਵਲੁ | Raag Bilaaval
Gurbani (795-831)
Ashtpadiyan (831-838)
Thitteen (838-840)
Vaar Sat (841-843)
Chhant (843-848)
Vaar Bilaaval (849-855)
Bhagat Bani (855-858)
ਰਾਗੁ ਗੋਂਡ | Raag Gond
Gurbani (859-869)
Ashtpadiyan (869)
Bhagat Bani (870-875)
ਰਾਗੁ ਰਾਮਕਲੀ | Raag Ramkalee
Ashtpadiyan (902-916)
Gurbani (876-902)
Anand (917-922)
Sadd (923-924)
Chhant (924-929)
Dakhnee (929-938)
Sidh Gosat (938-946)
Vaar Ramkalee (947-968)
ਰਾਗੁ ਨਟ ਨਾਰਾਇਨ | Raag Nat Narayan
Gurbani (975-980)
Ashtpadiyan (980-983)
ਰਾਗੁ ਮਾਲੀ ਗਉੜਾ | Raag Maalee Gauraa
Gurbani (984-988)
Bhagat Bani (988)
ਰਾਗੁ ਮਾਰੂ | Raag Maaroo
Gurbani (889-1008)
Ashtpadiyan (1008-1014)
Kaafee (1014-1016)
Ashtpadiyan (1016-1019)
Anjulian (1019-1020)
Solhe (1020-1033)
Dakhni (1033-1043)
ਰਾਗੁ ਤੁਖਾਰੀ | Raag Tukhaari
Bara Maha (1107-1110)
Chhant (1110-1117)
ਰਾਗੁ ਕੇਦਾਰਾ | Raag Kedara
Gurbani (1118-1123)
Bhagat Bani (1123-1124)
ਰਾਗੁ ਭੈਰਉ | Raag Bhairo
Gurbani (1125-1152)
Partaal (1153)
Ashtpadiyan (1153-1167)
ਰਾਗੁ ਬਸੰਤੁ | Raag Basant
Gurbani (1168-1187)
Ashtpadiyan (1187-1193)
Vaar Basant (1193-1196)
ਰਾਗੁ ਸਾਰਗ | Raag Saarag
Gurbani (1197-1200)
Partaal (1200-1231)
Ashtpadiyan (1232-1236)
Chhant (1236-1237)
Vaar Saarang (1237-1253)
ਰਾਗੁ ਮਲਾਰ | Raag Malaar
Gurbani (1254-1293)
Partaal (1265-1273)
Ashtpadiyan (1273-1278)
Chhant (1278)
Vaar Malaar (1278-91)
Bhagat Bani (1292-93)
ਰਾਗੁ ਕਾਨੜਾ | Raag Kaanraa
Gurbani (1294-96)
Partaal (1296-1318)
Ashtpadiyan (1308-1312)
Chhant (1312)
Vaar Kaanraa
Bhagat Bani (1318)
ਰਾਗੁ ਕਲਿਆਨ | Raag Kalyaan
Gurbani (1319-23)
Ashtpadiyan (1323-26)
ਰਾਗੁ ਪ੍ਰਭਾਤੀ | Raag Prabhaatee
Gurbani (1327-1341)
Ashtpadiyan (1342-51)
ਰਾਗੁ ਜੈਜਾਵੰਤੀ | Raag Jaijaiwanti
Gurbani (1352-53)
Salok | Gatha | Phunahe | Chaubole | Swayiye
Sehskritee Mahala 1
Sehskritee Mahala 5
Gaathaa Mahala 5
Phunhay Mahala 5
Chaubolae Mahala 5
Shaloks Bhagat Kabir
Shaloks Sheikh Farid
Swaiyyae Mahala 5
Swaiyyae in Praise of Gurus
Shaloks in Addition To Vaars
Shalok Ninth Mehl
Mundavanee Mehl 5
ਰਾਗ ਮਾਲਾ, Raag Maalaa
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Health & Nutrition
Slow Metabolism 'obesity Excuse' True
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<blockquote data-quote="spnadmin" data-source="post: 192576" data-attributes="member: 35"><p><strong>Slow metabolism 'obesity excuse' true</strong></p><p></p><p>By James Gallagher Health </p><p></p><p><a href="http://www.bbc.co.uk/news/health-24610296" target="_blank">http://www.bbc.co.uk/news/health-24610296</a></p><p></p><p>The mocked "obesity excuse" of being born with a slow metabolism is actually true for some people, say researchers.</p><p></p><p>A team at the University of Cambridge has found the first proof that mutated DNA does indeed slow metabolism.</p><p></p><p>The researchers say fewer than one in 100 people are affected and are often severely obese by early childhood.</p><p></p><p>The findings, published in the journal Cell, may lead to new obesity treatments even for people without the mutation.</p><p></p><p>Scientists at the Institute of Metabolic Science, in Cambridge, knew that mice born without a section of DNA, a gene called KSR2, gained weight more easily.</p><p></p><p>But they did not know what effect it may be having in people, so they analysed the DNA of 2,101 severely obese patients.</p><p></p><p>Some had mutated versions of KSR2.</p><p></p><p>It had a twin effect of increasing their appetite while their slowing metabolism.</p><p></p><p>"You would be hungry and wanting to eat a lot, you would not want to move because of a slower metabolism and would probably also develop type 2 diabetes at a young age," lead researcher Prof Sadaf Farooqi told the BBC.</p><p></p><p>She added: "It slows the ability to burn calories and that's important as it's a new explanation for obesity."</p><p></p><p>The mutation delivers a double-whammy by increasing the drive to eat and reducing calorie burn</p><p></p><p>Rare</p><p></p><p>KSR2 is mostly active in the brain and it affects the way individual cells interpret signals, such as the hormone insulin, from the blood. This in turn affects the body's ability to burn calories.</p><p></p><p>Prof Farooqi said the metabolism argument had been derided by doctors, as well as wider society, due to a lack of evidence that metabolism was slowed in obese patients. In many cases obese patients have an elevated metabolism to cope with fuelling a much larger body.</p><p></p><p>She said less than 1% of people had mutated versions of the gene and some would be a normal weight, but about 2% of children who were obese by the age of five would have the mutated gene.</p><p></p><p>However, if drugs could be developed to target problems with KSR2, then it might be beneficial to anyone who is too fat.</p><p></p><p>"Other genetic disorders, such as in blood pressure, have shown that even where there's a normal gene, targeting the pathway can still help," Prof Farooqi said.</p><p></p><p>The amount and types of food eaten, as well as levels of exercise, directly affect weight, but some people at more risk of becoming obese that others.</p><p></p><p>Obesity can run in families. The other obesity genes that have been discovered tend to affect appetite.</p><p></p><p>People have two copies of the FTO gene - one from each parent - and each copy comes in a high- and a low-risk form. Those with two-high risk copies of the FTO gene are thought to be 70% more likely to become obese than those with low-risk genes.</p><p></p><p>It makes fatty foods more tempting and alters levels of the hunger hormone ghrelin.</p><p></p><p>Dr Katarina Kos, from the University of Exeter Medical School, said: "It is an exciting and interesting breakthrough, this is a new pathway predisposing people to obesity.</p><p></p><p>"But it does exist in obese and lean people so you still need the obesogenic environment."</p></blockquote><p></p>
[QUOTE="spnadmin, post: 192576, member: 35"] [B]Slow metabolism 'obesity excuse' true[/B] By James Gallagher Health [url]http://www.bbc.co.uk/news/health-24610296[/url] The mocked "obesity excuse" of being born with a slow metabolism is actually true for some people, say researchers. A team at the University of Cambridge has found the first proof that mutated DNA does indeed slow metabolism. The researchers say fewer than one in 100 people are affected and are often severely obese by early childhood. The findings, published in the journal Cell, may lead to new obesity treatments even for people without the mutation. Scientists at the Institute of Metabolic Science, in Cambridge, knew that mice born without a section of DNA, a gene called KSR2, gained weight more easily. But they did not know what effect it may be having in people, so they analysed the DNA of 2,101 severely obese patients. Some had mutated versions of KSR2. It had a twin effect of increasing their appetite while their slowing metabolism. "You would be hungry and wanting to eat a lot, you would not want to move because of a slower metabolism and would probably also develop type 2 diabetes at a young age," lead researcher Prof Sadaf Farooqi told the BBC. She added: "It slows the ability to burn calories and that's important as it's a new explanation for obesity." The mutation delivers a double-whammy by increasing the drive to eat and reducing calorie burn Rare KSR2 is mostly active in the brain and it affects the way individual cells interpret signals, such as the hormone insulin, from the blood. This in turn affects the body's ability to burn calories. Prof Farooqi said the metabolism argument had been derided by doctors, as well as wider society, due to a lack of evidence that metabolism was slowed in obese patients. In many cases obese patients have an elevated metabolism to cope with fuelling a much larger body. She said less than 1% of people had mutated versions of the gene and some would be a normal weight, but about 2% of children who were obese by the age of five would have the mutated gene. However, if drugs could be developed to target problems with KSR2, then it might be beneficial to anyone who is too fat. "Other genetic disorders, such as in blood pressure, have shown that even where there's a normal gene, targeting the pathway can still help," Prof Farooqi said. The amount and types of food eaten, as well as levels of exercise, directly affect weight, but some people at more risk of becoming obese that others. Obesity can run in families. The other obesity genes that have been discovered tend to affect appetite. People have two copies of the FTO gene - one from each parent - and each copy comes in a high- and a low-risk form. Those with two-high risk copies of the FTO gene are thought to be 70% more likely to become obese than those with low-risk genes. It makes fatty foods more tempting and alters levels of the hunger hormone ghrelin. Dr Katarina Kos, from the University of Exeter Medical School, said: "It is an exciting and interesting breakthrough, this is a new pathway predisposing people to obesity. "But it does exist in obese and lean people so you still need the obesogenic environment." [/QUOTE]
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